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Decreased acid secretion and gastric lesion production by morphine in rats

Insights

Morphine, at pain-relieving doses, reduces gastric secretion and causes stomach lesions in rats. Naloxone, an opiate antagonist, reversed these effects, suggesting opiate receptor involvement.

Area of Science:

  • Pharmacology
  • Gastroenterology
  • Neuroscience

Background:

  • Opioid analgesics like morphine are widely used for pain management.
  • Morphine's effects on the gastrointestinal system, particularly gastric secretion and mucosal integrity, are not fully understood.
  • Opiate receptors are known to play roles in various physiological processes, including pain and gastrointestinal function.

Purpose of the Study:

  • To investigate the impact of graded doses of morphine on gastric secretion in conscious rats.
  • To determine if morphine induces gastric mucosal lesions and if these effects are dose-dependent.
  • To explore the role of opiate receptors in mediating morphine's effects on gastric function and ulcerogenicity.

Main Methods:

  • Conscious rats underwent pyloric occlusion to collect gastric secretions.
  • Graded doses of morphine were administered, and effects on gastric volume and acid output were measured.
  • Gastric mucosal lesions were assessed in a dose-dependent manner.
  • Rats were pretreated with naloxone (an opiate receptor antagonist) to evaluate its effect on morphine-induced gastric changes.

Main Results:

  • Morphine significantly decreased gastric secretion volume and total acid output at doses that also prolonged reaction time in the tail-immersion test.
  • Morphine administration resulted in dose-dependent gastric mucosal lesions.
  • Pretreatment with naloxone (4 mg/kg) significantly alleviated the gastric effects induced by morphine (32 mg/kg).

Conclusions:

  • Morphine exerts a dose-dependent inhibitory effect on gastric secretion in rats.
  • Morphine exhibits ulcerogenic properties, inducing gastric mucosal lesions.
  • The findings suggest that the effects of morphine on gastric secretion and its ulcerogenicity are mediated through stimulation of opiate receptors, as evidenced by naloxone's antagonistic action.

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